scholarly journals Voltage-sensitive potassium channels in Limulus ventral photoreceptors.

1978 ◽  
Vol 71 (1) ◽  
pp. 101-120 ◽  
Author(s):  
J S Pepose ◽  
J E Lisman
Keyword(s):  
Functional Role ◽  
Resting Potential ◽  
Reverse Direction ◽  
Voltage Range ◽  
K Channels ◽  
Response Intensity ◽  
Intracellular Injection ◽  
Voltage Dependent ◽  
Ionic Basis

The steady-state slope conductance of Limulus ventral photoreceptors increases markedly when the membrane is depolarized from rest. The ionic basis of this rectification has been examined with a voltage-clamp technique. Tail currents that occur when membrane potential is repolarized after having been depolarized have been identified. The tail currents reverse direction at a voltage that becomes more positive when Ko is increased. Rectification is reduced by extracellular 4-aminopyridine and by intracellular injection of tetra-ethyl-ammonium (TEA). These results indicate that the membrane rectification around resting potential is due primarily to voltage-sensitive K+ channels. The increase in gK caused by depolarization is not mediated by a voltage-dependent rise in in Cai++, since intracellular injection of Ca++ causes a decrease rather than an increase in slope conductance. TEA can be used to examine the functional role of the K+ channels because it blocks them without substantially affecting the light-activated Na+ conductance. The effect of TEA on response-intensity curves shows that the K+ channels serve to compress the voltage range of receptor potentials.

Evolution of Adaptive Neural Networks: The Role of Voltage-Dependent K+ channels

1998 ◽  
Vol 119 (3) ◽  
pp. 204-211 ◽  
Author(s):  
Daniel L. Alkon ◽  
Antonella Favit ◽  
Thomas Nelson
Keyword(s):  
Neural Networks ◽  
K Channels ◽  
Adaptive Neural Networks ◽  
Voltage Dependent

Role of Endothelial K + Channels in NO-Dependent Vasorelaxant Responses to Acetylcholine in Rat Aorta.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 698-698
Author(s):  
John Quilley ◽  
Yue Qiu
Keyword(s):  
Dose Response ◽  
Response Curve ◽  
Rat Aorta ◽  
Dose Response Curve ◽  
Response Curves ◽  
K Channels ◽  
Voltage Dependent ◽  
The Right ◽  
Stimulation Of

P30 Endothelium-dependent vasorelaxant responses to acetylcholine (Ach) in rat aorta are mediated solely by NO. Rings precontracted with U46619 were used to investigate the role of endothelial K + channels. Thus, any effect of K + channel inhibitors on Ach responses in the absence of an effect on those to nitroprusside (NP) can be attributed to interference with Ach-induced stimulation of NO. Vasorelaxant responses to Ach (log EC 50 -7.29M) were abolished by removal of the endothelium or inhibition of NO synthesis with nitroarginine (100μM) which potentiated responses to NP (log EC 50 -9.41M vs -8.47M for control). In the presence of TEA (10mM) to inhibit K + channels, the dose-response curve for Ach, but not NP, was shifted to the right (log EC 50 -6.06). Elevation of extracellular K + (25mM KCl)also shifted the dose-response curve for Ach to the right. Inhibitors of specific types of K + channels: BaCl 2 (30μM), apamin (100nM), glibenclamide (10μM), charybdotoxin (50nM) and iberiotoxin (100nM) were without effect on dose-response curves to either Ach or NP. However, the combination of apamin (100nM) and charybdotoxin (50nM) but not apamin plus iberiotoxin, reduced relaxant responses to Ach (log EC 50 -6.95M) without affecting those to NP.These results confirm that Ach-induced relaxation of rat aorta is mediated entirely by endothelium-derived NO, the release of which apparently involves hyperpolarization of the endothelium. This effect is dependent on activation of a K + channel that is blocked by a combination of apamin/charybdotoxin but neither agent alone, possibly indicating characteristics of both Ca 2+ - activated and voltage-dependent K + channels.

The Functional Role of Alternative Splicing of Ca2+-Activated K+ Channels in Auditory Hair Cells

1999 ◽  
Vol 868 (1 MOLECULAR AND) ◽  
pp. 379-385 ◽  
Author(s):  
E.M. C. JONES ◽  
M. GRAY-KELLER ◽  
J. J. ART ◽  
R. FETTIPLACE
Keyword(s):  
Alternative Splicing ◽  
Hair Cells ◽  
Functional Role ◽  
Auditory Hair Cells ◽  
K Channels

LOCAL ELECTRONIC PROPERTIES OF DOMAIN BOUNDARIES ON c(2 × 2) Fe(001) THIN FILM SURFACES

2006 ◽  
Vol 05 (06) ◽  
pp. 935-942 ◽  
Author(s):  
HIROFUMI OKA ◽  
AGUS SUBAGYO ◽  
KAZUHISA SUEOKA
Keyword(s):  
Bias Voltage ◽  
Surface States ◽  
Scanning Tunneling ◽  
Tunneling Conductance ◽  
Tunneling Microscopy ◽  
Voltage Range ◽  
Domain Boundaries ◽  
Voltage Dependent ◽  
The Difference

Scanning tunneling microscopy (STM) and spectroscopy have been performed on a nanostructure "line-like pattern" appearing on atomically flat terraces of bcc-Fe (001) with a c(2 × 2) reconstructed structure. Atomically resolved STM reveals that the line-like pattern consists of regularly aligned surface atoms that have a similar symmetry to the (1 × 1) structure of Fe (001). The line-like pattern plays a role of domain boundaries of c(2 × 2) domains. The patterns exhibit bias-voltage dependent image contrast in the STM topographic images. In negative sample bias-voltage range the patterns appear lower than the c(2 × 2) domains and higher in positive range. In dI/dV tunneling spectra taken on the patterns a shoulder is observed around +0.2 V. On the other hands, a small salient is distinguished around +0.4 V in the spectra taken on the c(2 × 2) domains. These features are originated from surface states existing on bcc-Fe (001) surfaces with (1 × 1) structure and c(2 × 2) reconstructed structure, respectively. Emergence of the line-like patterns results in the difference of tunneling conductance.

Local Anesthetics Modulate Neuronal Calcium Signaling through Multiple Sites of Action

2003 ◽  
Vol 98 (5) ◽  
pp. 1139-1146 ◽  
Author(s):  
Fang Xu ◽  
Zayra Garavito-Aguilar ◽  
Esperanza Recio-Pinto ◽  
Jin Zhang ◽  
Thomas J. J. Blanck
Keyword(s):  
Local Anesthetics ◽  
K Channel ◽  
Na Channels ◽  
Channel Blockade ◽  
K Channels ◽  
Voltage Dependent ◽  
Sites Of Action ◽  
A Site ◽  
Ca2 Channels

Background Local anesthetics (LAs) are known to inhibit voltage-dependent Na+ channels, as well as K+ and Ca2+ channels, but with lower potency. Since cellular excitability and responsiveness are largely determined by intracellular Ca2+ availability, sites along the Ca2+ signaling pathways may be targets of LAs. This study was aimed to investigate the LA effects on depolarization and receptor-mediated intracellular Ca2+ changes and to examine the role of Na+ and K+ channels in such functional responses. Methods Effects of bupivacaine, ropivacaine, mepivacaine, and lidocaine (0.1-2.3 mm) on evoked [Ca2+](i) transients were investigated in neuronal SH-SY5Y cell suspensions using Fura-2 as the intracellular Ca2+ indicator. Potassium chloride (KCl, 100 mm) and carbachol (1 mm) were individually or sequentially applied to evoke increases in intracellular Ca2+. Coapplication of LA and Na+/K+ channel blockers was used to evaluate the role of Na+ and K+ channels in the LA effect on the evoked [Ca2+](i) transients. Results All four LAs concentration-dependently inhibited both KCl- and carbachol-evoked [Ca2+](i) transients with the potency order bupivacaine > ropivacaine > lidocaine >/= mepivacaine. The carbachol-evoked [Ca2+](i) transients were more sensitive to LAs without than with a KCl prestimulation, whereas the LA-effect on the KCl-evoked [Ca2+](i) transients was not uniformly affected by a carbachol prestimulation. Na+ channel blockade did not alter the evoked [Ca2+](i) transients with or without a LA. In the absence of LA, K+ channel blockade increased the KCl-, but decreased the carbachol-evoked [Ca2+](i) transients. A coapplication of LA and K+ channel blocker resulted in larger inhibition of both KCl- and carbachol-evoked [Ca2+](i) transients than by LA alone. Conclusions Different and overlapping sites of action of LAs are involved in inhibiting the KCl- and carbachol-evoked [Ca2+](i) transients, including voltage-dependent Ca2+ channels, a site associated with the caffeine-sensitive Ca2+ store and a possible site associated with the IP(3)-sensitive Ca2+ store, and a site in the muscarinic pathway. K+ channels, but not Na+ channels, seem to modulate the evoked [Ca2+](i) transients, as well as the LA-effects on such responses.

scholarly journals The Insensitivity of TASK-3 K2P Channels to External Tetraethylammonium (TEA) Partially Depends on the Cap Structure

2018 ◽  
Vol 19 (8) ◽  
pp. 2437 ◽  
Author(s):  
Guierdy Concha ◽  
Daniel Bustos ◽  
Rafael Zúñiga ◽  
Marcelo Catalán ◽  
Leandro Zúñiga
Keyword(s):  
Functional Role ◽  
Simulation Analysis ◽  
K Channel ◽  
Channel Blockers ◽  
Tyrosine Residue ◽  
K Channels ◽  
Enhanced Sensitivity ◽  
K2p Channels ◽  
Pore Domain

Two-pore domain K+ channels (K2P) display a characteristic extracellular cap structure formed by two M1-P1 linkers, the functional role of which is poorly understood. It has been proposed that the presence of the cap explains the insensitivity of K2P channels to several K+ channel blockers including tetraethylammonium (TEA). We have explored this hypothesis using mutagenesis and functional analysis, followed by molecular simulations. Our results show that the deletion of the cap structure of TASK-3 (TWIK-related acid-sensitive K+ channel) generates a TEA-sensitive channel with an IC50 of 11.8 ± 0.4 mM. The enhanced sensitivity to TEA displayed by the cap-less channel is also explained by the presence of an extra tyrosine residue at position 99. These results were corroborated by molecular simulation analysis, which shows an increased stability in the binding of TEA to the cap-less channel when a ring of four tyrosine is present at the external entrance of the permeation pathway. Consistently, Y99A or Y205A single-residue mutants generated in a cap-less channel backbone resulted in TASK-3 channels with low affinity to external TEA.

Characterization and regulation of Ca2+-dependent K+ channels in human esophageal smooth muscle

1999 ◽  
Vol 276 (4) ◽  
pp. G843-G852 ◽  
Author(s):  
Bernard R. Hurley ◽  
Harold G. Preiksaitis ◽  
Stephen M. Sims
Keyword(s):  
Smooth Muscle ◽  
Patch Clamp ◽  
Functional Role ◽  
Channel Activity ◽  
Patch Clamp Recording ◽  
Channel Activation ◽  
Voltage Dependent ◽  
Human Esophagus ◽  
Current Reversal

We examined the properties of K+ channels in smooth muscle cells dissociated from human esophagus using patch-clamp recording in the cell-attached configuration. The predominant channel observed had a conductance of 224 ± 4 pS, and current reversal was dependent on K+ concentration. Channel activity was voltage dependent and increased with elevation of intracellular free Ca2+ concentration ([Ca2+]i), consistent with this being the large-conductance Ca2+-dependent K+(KCa) channel. ACh as well as caffeine caused transient increases in KCa channel activity, and the effects of ACh persisted in Ca2+-free solution, indicating that Ca2+ release from stores contributed to channel activation. Simultaneous patch clamp and fluorescence revealed that KCachannel activity was well correlated with elevation of [Ca2+]i. The functional role of KCachannels in esophagus was studied by measuring ACh-induced contraction of strips of muscle. Tetraethylammonium and iberiotoxin, blockers of KCa channels, increased ACh-induced contraction, consistent with a role for K+ channels in limiting excitation and contraction. These studies are the first to characterize KCa channels and their regulation in human esophageal smooth muscle.

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